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Phase 3B > Oncology > Flashcards

Oncology Flashcards

1
Q

What are cancer cells?

A

Cells which undergo uncontrolled and unregulated cell proliferation with the ability to metastasise to other places in the body.

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2
Q

What are the twelve characteristics of cancer cells that underline their behaviour?

A
  • Self sufficiency in growth signals
  • Insensitivity to anti-growth signals
  • Evading apoptosis
  • Limitless replicative potential
  • Sustained angiography
  • Tissue invasion and metastasis
  • Dysregulating metabolism
  • Evading the immune system
  • Genome instability
  • Inflammation
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3
Q

Where in the cell cycle do cytotoxic chemotherapy agents target?

A

Depends on how the agent works.
More rapidly growing tumours have more cycles and therefore more G1, S, and G2 phases.
So a drug specific for DNA synthesis (S) stage is most effective against rapidly growing tumours.

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4
Q

Define pharmacokinetics.

A

What the body does to the drug.

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5
Q

Define pharmacodynamics.

A

What the drug does to the body.

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6
Q

What are the main principles of cancer drug treatment?

A

The drug must reach the cancer cells
Cell must be sensitive to the cytotoxic of drug
Toxic effect must be minimal to the benefit of the drug

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7
Q

What is screening?

A

A process of identifying apparently health people who may be at increased risk of a disease or conditions.

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8
Q

How is the grade of a tumour determined?

A

The extent to which the neoplasm resembles its cell or tissue of origin.

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9
Q

How are malignant tumours graded?

A

Well, moderately, or poorly differentiated.

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10
Q

How are benign tumours graded?

A

They are not, as they closely resemble their parent tissue.

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11
Q

Which tumours grow slowly?

A

Well differentiated

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12
Q

What does the stage of a cancer describe?

A

The size of the tumour and the extent to which it has spread

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13
Q

What are the components of the TNM staging classification?

A

Tumour
Nodes
Metastases

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14
Q

What does TNM stage IV generally represent?

A

Metastases to distant organs

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15
Q

For which tumours is systemic anticancer treatment given alone, with radical intent?

A

Germ cell tumours

Haematological cancers

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16
Q

What do “neoadjuvant” and “adjuvant” mean?

A

Neoadjuvant - perioperative period, pre surgery

Adjuvant - perioperative, post surgery

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17
Q

Why does surgical resection of early tumours not cure some patients?

A

Presence of micrometastases which can cause recurrence.

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18
Q

How does neoadjuvant chemotherapy offer survival benefit?

A

Eradicated micrometastatic disease

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19
Q

What are the risks of neoadjuvant chemotherapy?

A

Risks a potentially fatal chemotherapy related complication.

Decreases the patients performance prior to curative surgery

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20
Q

Why is adjuvant chemotherapy given?

A

Ensures any margins or micrometastatic sites are free from disease

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21
Q

What is radiotherapy?

A

The administration of ionizing radiation with the intent of killing the cancer cell or prevent it from replicating.

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22
Q

How does radiotherapy work?

A

Ionizing - ionizes cells causing apoptosis
Non-ionizing (X-Rays) - formation of free radicals and reactive oxygen species. These interact with the covalent bonds of DNA and can result in apoptosis.

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23
Q

How is radiotherapy delivered?

A

External to the body
Internal to the body (brachytherapy)
Systemically (iodine-131)

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24
Q

What is the radiation dose measured in?

A

Grays - Gy

The amount of radiation absorbed by each kilogram of tissue

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25
Q

What are the acute side effects of radiotherapy?

A 
Nausea, vomiting, anorexia
Acute radiation dermatitis
Mucositis
Oesophagitis
Diarrhoea
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26
Q

Name three types of systemic anti-cancer treatment.

A

Cytotoxic chemotherapy
Hormone therapy
Molecularly targeted therapy

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27
Q

How are cytotoxic chemotherapies classified?

A

Alkylating agents
Antimetabolites
Natural products

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28
Q

How do alkylating agents work?

A

Add an alkyl group to the guanine base of DNA, preventing DNA replication and RNA transcription.
Not phase specific i.e. can occur at any point in the cell cycle

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29
Q

How do antimetabolites work?

A

Inhibit enzymes or metabolites involved in DNA or RNA synthesis

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30
Q

Name two alkylating agents

A

Cisplatin

Cyclophosphamide

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31
Q

Name two antimetabolites

A

Methotrexate

Fluorouracil

32
Q

Name two natural products

A

Bleomycin

Doxorubicin

33
Q

What are some problems with chemotherapy?

A

Variable efficacy secondary to tumour biology/intrinsic resistance
Acquired resistance
Toxic side effects

34
Q

What are general side effects of chemotherapy related to?

A

Rapidly dividing cells

35
Q

Name some general side effects of chemotherapy.

A

Nausea and vomiting
Alopecia
Skin rashes
Constipation

36
Q

Name some other specific side effects of chemotherapy?

A

Cardiomyopathy
Renal impairment
Infertility

37
Q

Define hypercalcaemia.

A

Corrected calcium >2.6mmol/L

38
Q

40% of circulating calcium is bound to what?

A

Albumin

39
Q

How do you correct calcium levels?

A

Add 0.1mmol/L to calcium, for every 4g/L that albumin levels are below 40g/L

This allows for changes in serum albumin levels

40
Q

What are the main causes of hypercalcaemia?

A

Hyperparathyroidism
Malignancy - bone mets or parathyroid hormone related peptide secretion
Thyrotoxicosis

41
Q

How does hypercalcaemia present?

A

Bones, stones, groans, and psychic moans

Abdo pain, constipation, vomiting
Polyuria and polydipsia
Confusion and fatigue
Depression

42
Q

What are the important investigations for hypercalcaemia?

A

PTH
ECG
Imaging for bone mets if appropriate

43
Q

What is seen on ECG in hypercalcaemia?

A

Shortened QT interval

44
Q

What is the initial acute management of hypercalcaemia?

A

Diagnose underlying cause

Correct dehydration with 0.9% saline

45
Q

What is the further management of hypercalcaemia following rehydration?

A

IV bisphosphonates e.g. pamidronate

Inhibits osteoclasts and reduces bone turnover, reduces calcium over several days

46
Q

What is the treatment of persistent or relapsed hypercalcaemia of malignancy?

A

Denosumab (inhibits RANK ligand)

47
Q

What does the SVC drain?

A

The head, neck, upper limbs, and upper thorax

48
Q

What are the causes of SVC obstruction?

A

Thrombus

Direct tumour invasion inside and outside the vessel wall

49
Q

Which tumours can invade the SVC?

A

Lung cancer
Lymphoma
Germ cell tumours
ALL

50
Q

What are the symptoms of SVC obstruction?

A 
May be sudden or gradual
Dyspnoea
Chest pain at rest
Cough
Neck, face, and arm swelling
Nasal stuffiness
Visual disturbance
51
Q

What are the signs of SVC obstruction?

A

Dilated veins and oedema over arms, neck, and anterior chest wall
Severe respiratory distress
Cyanosis
Engorged conjunctiva

52
Q

How is SVC obstruction diagnosed?

A

Clinical
CXR - widened mediastinum/mass
CT

53
Q

How is SVC obstruction managed?

A

Elevation of the head, oxygen
High dose dexamethasone
Endovascular stenting

54
Q

What is the name of the condition caused by abrupt release of large quantities of cellular components into the blood following rapid lysis of the malignant cell?

A

Tumour lysis syndrome

55
Q

What are the risk factors for tumour lysis syndrome?

A

Volume depletion
Renal impairment
Treatment sensitive tumours
High pre-treatment urate, lactate, and LDH

56
Q

What are the most common malignancies for tumour lysis syndrome?

A

Haematological

57
Q

How does tumour lysis syndrome present?

A

Weakness
Paralytic ileus - constipation, vomiting, abdo pain
Cardiac arrhythmias - palpitations, chest pain
Seizures
AKI

58
Q

What are the metabolic abnormalities of tumour lysis syndrome?

A 
Hyperuricaemia
Hyperphosphataemia
Hyperkalaemia
Hypocalcaemia
AKI
59
Q

How does tumour lysis syndrome cause renal impairment?

A

Deposition of uric acid and calcium phosphate crystals in renal tubules can cause acute renal failure

60
Q

How is tumour lysis syndrome prevented?

A

IV fluids
Allopurinol
Rasburicase

61
Q

How does allopurinol work?

A

Xanthine oxidase inhibitor

Blocks conversion of xanthines to uric acid

62
Q

How does rasburicase work?

A

Recombinant urate oxidase

Catalyses the oxidation of uric acid to allantoin which is much more soluble

63
Q

How is tumour lysis syndrome treated?

A 
Vigorous hydration
Correct high potassium
Rasburicase (stop allopurinol)
Acetazolamide
Phosphate binders
Dialysis
64
Q

How is potassium corrected in tumour lysis syndrome?

A

10mls 10% calcium gluconate IV if potassium >7mmol/L or ECH changes
IV insulin and dextrose
Salbutamol 2.5mg nebulizer

65
Q

Which patients are at risk of neutropenic sepsis?

A

Neutrophil count below 1x10^9/L

66
Q

When should patients be treated for neutropenic sepsis?

A

Oral temperature >38 degrees OR
Two consecutive readings of >37.5 degrees for two hours
AND an absolute neutrophil count <1x10^9/L

67
Q

How is neutropenic sepsis diagnosed?

A

Septic screen

Clinically relevant swabs or cultures

68
Q

What are the antibiotic guidelines for neutropenic sepsis?

A

Piperacillin with tazobactam - tazocin

69
Q

How is neutropenic sepsis prevented against?

A

Fluoroquinolone or granulocyte colony stimulating factor in some cases

70
Q

Where does the spinal cord run to and from?

A

The base of the skull to L1

71
Q

What does the cauda equina contain?

A

Extends below L1 and contains the lumbar, sacral, and coccygeal spinal nerves

72
Q

What is the most common cause of spinal cord compression?

A

Secondary malignancy

73
Q

What are the other causes of spinal cord compression?

A

Trauma
Disc prolapse
RA
Spinal infection

74
Q

How does spinal cord compression present?

A

Radicular pain
Limb weakness below the level of compression
Sensory loss below level of compression (sensory level present)
Bladder or bowel dysfunction

75
Q

How is spinal cord compression diagnosed?

A

MRI whole spine

76
Q

How is spinal cord compression treated?

A

Analgesia
High dose steroids
Spinal decompression
Radiotherapy

Phase 3B (20 decks)

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